Type 1 diabetes (T1DM) is caused by autoimmune destruction of β -cells that produce insulin. Although exogenous insulin is widely used, the affected people cannot continue to achieve satisfactory results through the current formula and technology, so they still face the risk of acute and long -term complications.
Earlier researchers have conducted a series of clinical trials with various immunotherapy to protect the β -cell function of recently onset of T1DM patients. Although there are these research work, it has not achieved strong success: the two -phase study of a small number of large placebo comparisons has reached the main end point, but patients who receive treatment usually must continue to use exogenous insulin, and with the exit of the treatment method, the treatment method withdraws from the withdrawal method. The effect of immunotherapy will gradually weaken.
Therefore, researchers continue to find new therapies that prevent β cells from destruction, and pay special attention to re -use drugs that have been approved for other indications, thereby accelerating its application in T1DM. In the process of exploration, Imaidinib (brand name Glevin, that is, “I am not a medicine god”) -The first type of TKI inhibitor, as a treatment method for chronic bone marrow leukemia, has already been treated Make significant success.
During clinical studies, Emantini was proven to prevent diabetes in non -obesity diabetes (NOD) mice. Further clinical survey shows that Imadinib may play a role through new metabolic channels, such as offsetting the high -level internal quality network (ER) pressure of β cells, reducing apoptosis and improving insulin sensitivity.
Recently, experts from San Francisco University in the United States have carried out relevant research to evaluate the safety and effectiveness of Imaidinib in protecting the function of β cells in T1DM patients who have developed recently. The results were published in the Lancet Diabetes & Endocrinology.
Researchers conducted a two -stage test of multi -center, random, double -blindness, and placebo control. Nine medical centers from the United States (N = 8) and Australia (N = 1) recruited recently developed T1DM patients (after diagnosis 0.2nmol L-1.
Participants are randomly assigned (2: 1) to receive 400mg Imaidinib or matching placebo for 26 weeks. The blocking random scheme generated by a computer is layered according to the center. The main end point is the difference between the average value of the curve (AUC) average of the Imaidinib and the placebo group of the MMTT 2 hours before the 12 -month MMTT. And further observe until 24 months.
45 patients were allocated to accept Imaidinib and 22 accepted placebo. In the end, the 43 participants and the placebo group of the Imarinib group were included in the main ITT analysis of 12 months. The study reached the main end point: the average difference between Ima Diitinib and placebo therapy at 12 hours C -peptide AUC was 0.095. But this effect does not last for 24 months.
During the 24 -month follow -up, 32 of the 45 participants who were treated with Imaidinib (71%) had level 2 or more serious adverse events. 13 people (59%). The most common adverse events between the two groups are gastrointestinal problems (6 people [13%]).
In summary, the 26 weeks of Emartinib can retain the β -cell function of type 1 diabetic patients in 12 months. Emutinib may provide a new way to change the course of diabetic disease.
<!-2586: Diabetic terminal page
Imatinib therapy for patients with recent-onset type 1 diabetes： a multicentre， randomised， double-blind， placebo-controlled， phase 2 trial. https：//doi.org/10.1016/S2213-8587(21)00139-X